What it is:The process of finding patients who are malnourished or at risk, figuring out what they actually need, and picking a route (mouth, tube, or vein) to get it into them safely.
The core problem:Malnutrition isn't just "not eating enough." It's a mismatch between what the body needs and what it's getting, and that mismatch can come from poor intake (marasmus-type starvation) or from a body in a hypermetabolic, inflamed state that's burning through nutrients faster than they can be replaced (disease-related malnutrition from burns, trauma, sepsis, cancer, or chronic inflammatory disease). Both undernutrition and overnutrition wreck cellular and organ function and raise morbidity and mortality.
What you do about it:Screen everyone, assess the ones who screen positive, calculate their actual calorie/protein/fluid targets, and if they can't eat enough on their own, feed the gut before you feed the vein.
The organizing idea for this whole chapter is "does the gut work?"If yes, use enteral nutrition (EN), because it keeps the GI tract's structure and immune function intact and causes fewer infectious and technical complications than parenteral nutrition (PN). If no, or if EN alone can't meet needs, PN bypasses the gut entirely by going straight into a vein, at the cost of more risk and more cost. Every access and formulation decision downstream of this chapter is really just working out the details of that one branch point.
Malnutrition is an umbrella term for nutrient imbalance, and it covers both ends of the spectrum: undernutrition and overnutrition (obesity, covered separately in Chapter 59). There are two distinct undernutrition patterns worth telling apart because they come from different mechanisms.
| Type | Driven by | Typical picture |
|---|---|---|
| Marasmus (starvation-related) | Inadequate intake, absorption, or utilization of protein and calories, with no major inflammatory driver | Chronic wasting, low body weight, relatively preserved visceral proteins early on |
| Disease-related malnutrition | Increased metabolic demand from acute severe illness/injury (major infection, burns, trauma) or chronic inflammatory disease (Crohn's, organ failure, cancer) | Rapid protein losses, inflammation-driven catabolism, visceral proteins fall fast because the liver stops making them and starts making acute-phase reactants instead |
A patient losing weight from poor oral intake alone responds differently to feeding than a septic, inflamed patient. In the inflamed patient, you can pour in calories and protein and the labs (like albumin) may still look terrible, because inflammation itself, not lack of nutrition, is suppressing hepatic protein synthesis. Don't mistake a low albumin for a nutrition problem you can fix with more feeding if the real driver is unresolved inflammation.
Nutrition screening is the first filter: a quick, systematic check applied to everyone in a care setting to flag who might be malnourished or at risk, so that the ones who screen positive get a full nutrition assessment. That assessment is the actual foundation of the nutrition care plan, and it has three goals: find risk factors for malnutrition and its complications, estimate what the patient actually needs, and set baseline numbers you can use later to tell if therapy is working.
A full assessment pulls from medical, surgical, and dietary history plus a nutrition-focused physical exam (NFPE), a head-to-toe, system-based exam looking for abnormal nutrition-related findings in each body region. Underneath that exam sit four practical domains.
These are physical measurements (weight, stature, head circumference under age 3, waist circumference, and in select patients skinfold thickness, mid-arm muscle circumference, wrist circumference, or bioelectrical impedance analysis) compared against population norms.
Cheap, noninvasive, estimates lean body mass and total body water by exploiting the fact that fat and lean tissue conduct electricity differently. The catch: hydration status skews the result, and there's no current guideline recommendation to use it routinely in clinical practice.
These proteins are hepatic synthesis products, and their levels reflect a lot more than nutrition status: age, kidney losses (nephrotic syndrome), GI losses (protein-losing enteropathy), skin losses (burns), hydration (dehydration concentrates them, overhydration dilutes them), liver synthetic capacity, and metabolic stress/inflammation (sepsis, trauma, surgery, infection all drive them down independent of intake). Always read them in the context of the whole clinical picture, never in isolation.
| Protein | Half-life | Function | ↑ with | ↓ with |
|---|---|---|---|---|
| Albumin | 18-20 days | Plasma oncotic pressure, small-molecule transport | Dehydration, anabolic steroids, insulin, infection | Fluid overload, edema, kidney or liver dysfunction, poor intake, burns, HF, cirrhosis, trauma, sepsis |
| Transferrin | 8-9 days | Binds and transports iron | Fe deficiency, pregnancy, hypoxia, chronic blood loss, estrogens | Chronic infection, cirrhosis, burns, enteropathies, nephrotic syndrome |
| Prealbumin (transthyretin) | 2-3 days | Binds T3/T4, retinol-binding protein carrier | Impaired kidney function | Cirrhosis, hepatitis, stress, surgery, inflammation, hyperthyroidism, zinc deficiency |
Because prealbumin's half-life is only 2-3 days, it's the one that actually moves fast enough to be useful for tracking short-term response to nutrition therapy in an acute setting. Albumin's 18-20 day half-life makes it a lagging, unreliable marker for anything happening this week, it's really an inflammation/illness-severity marker more than a nutrition marker. Don't chase a low albumin with more tube feeds and expect it to normalize quickly.
Nutrition status affects immunity directly and indirectly. Total lymphocyte countand delayed cutaneous hypersensitivitytesting (using recall antigens the patient was likely already sensitized to, most commonly mumps and Candida albicans) are the two classic tests, but both lack specificity, so they're supportive findings, not stand-alone diagnostic tools.
A blunted or absent response to those recall antigens (anergy) is associated with severe malnutrition. The encouraging part: immune responsiveness can be restored with adequate nutrition repletion, so it's a reversible finding, not a fixed one.
Ideally you'd assess a nutrient based on its actual biologic function, but practical assays are limited, so most testing just measures serum concentration of the nutrient itself.
Requirements are always patient-specific: age, sex, size, clinical condition, nutrition status, and activity level all move the target. You can use validated predictive equations, direct measurement, or, most simply, population-based calorie-per-kilogram estimates, the choice depends on how sick the patient is and what resources you have.
| Requirement | Target | Notes |
|---|---|---|
| Energy, healthy adult | 20-25 kcal ABW/kg/day | Minimal illness severity, normal nutrition status |
| Energy, children | ~130-150% of basal metabolic rate | Plus extra for activity and growth |
| Energy, increased demand | Above baseline estimate | Fever, sepsis, major surgery, trauma, burns, long-term growth failure, chronic conditions (BPD, congenital heart disease, cystic fibrosis) |
| Protein, adult | 0.8 g/kg/day | Standard healthy adult allowance |
| Protein, adult >60 yrs | 1.5 g/kg/day | Higher requirement with age |
| Protein, metabolic stress | 1.5-2 g/kg/day | Infection, trauma, surgery |
| Protein, burns | 2.5-3 g/kg/day | Highest protein demand state on this list |
| Fluid, adult | 30-40 mL/kg/day | Adjust up for GI losses, fever, sweating, hypermetabolism; adjust down for kidney/heart failure or hypoalbuminemic starvation |
| Fluid, child/preterm <10 kg | ≥100 mL/kg/day | Plus 50 mL/kg for each kg from 11-20 kg, plus 20 mL/kg for each kg >20 kg |
45-65% carbohydrate, 20-35% fat, 10-35% protein.Same general split applies to children, except infants need 40-50% of calories from fatfor neurodevelopment.
Fluid status monitoring:track urine output and specific gravity, serum electrolytes, and weight trends. Adequate tissue perfusion needs at least 1 mL/kg/hrurine output in children or 40-50 mL/hrin adults.
Micronutrients(electrolytes, minerals, trace elements, vitamins) shift with age, sex, route of intake, and underlying disease. In kidney failure, sodium, potassium, magnesium, and phosphorus requirements typically drop while calcium requirements rise.
Plenty of routine medications quietly deplete or block absorption of specific micronutrients, and some drug vehicles are themselves a nutrient source worth remembering (propofol's vehicle is a 10% lipid emulsion; most IV fluids carry dextrose or sodium).
| Drug / class | Effect |
|---|---|
| ACE inhibitors, ARBs | Increased urinary zinc losses |
| Thiazide diuretics | Increased urinary zinc losses |
| Antacids, loop diuretics | Thiamine deficiency |
| Cholestyramine, colestipol, orlistat | Malabsorption of fat-soluble vitamins A, D, E, K (and β-carotene) |
| Corticosteroids | Decreased vitamins A, D, C |
| H2 antagonists, PPIs | Reduced acid impairs vitamin B12 release from food; PPIs also reduce iron absorption |
| Isoniazid | Vitamin B6 and niacin deficiency |
| Phenytoin, phenobarbital, primidone | Increased vitamin D metabolism; phenytoin also lowers folic acid |
| Methotrexate, pentamidine, trimethoprim, sulfasalazine | Folic acid deficiency or malabsorption |
| Warfarin | Vitamin K antagonizes effect; vitamins A, C, E may alter prothrombin time |
| Zidovudine | Folic acid and B12 deficiency worsen myelosuppression |
| Isotretinoin | Vitamin A increases toxicity risk |
Acid-suppressing drugs (PPIs, H2RAs) block B12 release from food and reduce iron absorption. Bile-acid sequestrants and fat blockers (cholestyramine, colestipol, orlistat) take out the fat-soluble vitamins ADEK together because they all share the same absorption pathway. Anticonvulsants and antifolates hit folate. Grouping the interactions by mechanism, not memorizing each line separately, is what makes this table stick.
EN delivers nutrients by tube or mouth into a functioning GI tract; this chapter's focus is feeding-tube delivery. The goal is simple: supply the calories, macronutrients, and micronutrients a patient can't get from an adequate oral diet.
EN fits the patient who can't or won't eat enough to meet needs andhas both a working GI tract and a way to access it. Common triggers: neoplastic disease, organ dysfunction, hypermetabolic states, GI disease, neurologic impairment.
Distal mechanical intestinal obstruction, bowel ischemia, and necrotizing enterocolitisrule out EN entirely. Active peritonitis and uncorrectable coagulopathyrule out tube placementspecifically. Severe diarrhea, protracted vomiting, enteric fistulas, severe GI hemorrhage, hemodynamic instability, and intestinal dysmotility don't necessarily rule EN out, but they make success harder and need close attention.
EN has replaced PN as the preferred nutrition support method for critically ill patients who need specialized feeding, because it preserves GI structure and function and causes fewer metabolic, infectious, and technical complications, at lower cost.
In critically ill patients, starting EN within 24-48 hoursof ICU admission is linked to less disease severity and fewer infectious complications compared to starting after 48 hours. If a patient is only mildly to moderately stressed and was well-nourished going in, it's reasonable to hold off on EN until oral intake has been inadequate for 5-7 days.
Four access routes, chosen based on expected duration of use and whether the feeding site needs to be the stomach or the small bowel.
| Access | Best for | Advantage | Watch out for |
|---|---|---|---|
| Nasogastric / orogastric | Short term, intact gag reflex, normal gastric emptying | Easy bedside placement, cheap, supports all administration methods | Tube displacement, aspiration risk |
| Nasojejunal | Short term, impaired gastric emptying or high aspiration risk | Lower aspiration risk, allows early post-injury/post-op feeding | Harder to place, tube clogging/displacement, can't do bolus feeds |
| Gastrostomy | Long term (>4-6 weeks), normal gastric emptying | All administration methods, low-profile buttons available, large-bore tubes clog less | Procedural risk, stoma site complications, aspiration risk |
| Jejunostomy | Long term, impaired gastric emptying or high aspiration risk | Lower aspiration risk, early feeding possible | Procedural risk, stoma complications, can't do bolus feeds |
The stomach is the cheapest, least labor-intensive site, but patients with impaired gastric emptying risk aspiration pneumonia there. Once EN is expected to run past 4-6 weeks, switch thinking from a nasal tube to a gastrostomy or jejunostomy.
Bolus feeding is the most convenient but carries the highest risk of cramping, nausea, vomiting, aspiration, and diarrhea. Intermittent feeding mimics normal meal patterns like bolus does, just stretched out, which is what improves tolerance. Watch for the intolerance signs regardless of method: abdominal distention or cramping, high gastric residual volumes, aspiration, diarrhea. Standardized initiation/advancement protocols help hit nutrient goals without triggering these.
Formulas are built from a carbohydrate source (usually the main calorie source; polymeric carbs are preferred over simple/elemental sugars), a protein source (its molecular form determines how much digestion is needed before absorption), and a fat source (usually vegetable oils rich in polyunsaturated fatty acids). Many formulas also add soluble or insoluble fiber for trophic effects on the colon, better sodium/water absorption, and bowel regulation.
Adult EN formulas range 280-875 mOsm/kg. Osmolality is widely assumed to drive GI intolerance, but the evidence for that link is actually weak. Don't over-index on osmolality alone when troubleshooting a formula tolerance issue.
| Category | Key features | Use case |
|---|---|---|
| Standard polymeric | Isotonic, 1-1.2 kcal/mL, NPC:N 125:1-150:1 | Meets most patients' needs; functional GI tract |
| High protein | NPC:N <125:1 | Protein needs >1.5 g/kg/day: trauma, burns, pressure sores, wounds; also patients on propofol |
| High caloric density | 1.5-2 kcal/mL, hypertonic, lower electrolyte per calorie | Fluid/electrolyte restriction, e.g. kidney insufficiency |
| Elemental | High free amino acid content, low fat | Need for low fat; largely replaced by peptide-based formulas now |
| Peptide-based | Di/tripeptides, contains MCTs | Trial in malabsorption/intolerance to intact protein; benefit not firmly established |
| Disease-specific: renal | Caloric dense, low electrolyte, variable protein | Alternative to standard high-caloric formulas, pricier |
| Disease-specific: liver | ↑ branched-chain, ↓ aromatic amino acids | Hepatic encephalopathy |
| Disease-specific: lung | High fat, low carb, anti-inflammatory lipids/antioxidants | ARDS, severe acute lung injury |
| Disease-specific: diabetes | High fat, low carb | Alternative to standard fiber formula with uncontrolled hyperglycemia |
| Immune-modulating | Glutamine, arginine, nucleotides, omega-3s | Major elective GI surgery, trauma, burns, head/neck cancer, ventilated critically ill; use caution in sepsis |
| Oral supplement | Sweetened, hypertonic | Boosting an inadequate oral diet |
This comes up constantly on the floor. Solids that can safely be crushed (not sublingual, not sustained-release, not enteric-coated) or capsules that can be opened get mixed with 15-30 mLof water or another appropriate solvent. Otherwise, use a liquid dosage form. Give multiple medications separately, flushing with 5-15 mL waterbetween each.
Mixing liquid medications directly with EN formula risks physical incompatibility that blocks drug absorption and clogs small-bore tubes, especially with formulas containing intact (rather than hydrolyzed) protein and with acidic liquid medications. Avoid it whenever possible; give meds and formula separately.
| Drug | The interaction | What to do |
|---|---|---|
| Phenytoin | Possible binding to calcium caseinates/protein hydrolysates in the formula, lowers bioavailability | Hold feeds 1-2 hr before/after; adjust feeding rate to make up held time; monitor level and response closely; consider IV or an alternative if levels won't come up |
| Fluoroquinolones, tetracyclines | Complexation with divalent/trivalent cations in the formula lowers bioavailability | Hold feeds 1 hr before/after; avoid jejunal ciprofloxacin; monitor response |
| Warfarin | Decreased absorption from the feeding itself, plus vitamin K in the formula antagonizes effect | Adjust dose by INR; expect to raise dose when feeds start, lower it when they stop; consider holding feeds 1 hr before/after |
| Omeprazole, lansoprazole | Acid-labile drug in delayed-release granules that get sticky with water and clog small-bore tubes | Mix granules with acidic liquid for gastric tubes, or use an extemporaneous oral liquid suspension |
PN delivers macro- and micronutrients through a central or peripheral vein, bypassing the gut entirely. It's the option for a patient who can't meet nutrition needs enterally for an extended period, and it only enters the picture once EN has been ruled out or has fallen short.
| PPN (peripheral) | CPN (central) | |
|---|---|---|
| Candidate | Modest nutrient needs, not fluid restricted, GI function expected to return in 10-14 days | PN needed >7-14 days, large nutrient needs, poor peripheral access, or fluctuating fluid needs |
| Amino acid concentration | 3-5% | Higher, more concentrated |
| Dextrose concentration | 5-10% | Higher, hypertonic |
| Main advantage | Lower infectious and technical complication risk | Handles large or fluctuating nutrient/fluid demands |
| Main disadvantage | Can't meet large nutrient needs; limited by peripheral vein tolerance | Catheter insertion, use, and infection risk; PICCs commonly used for short- or long-term access |
PPN solutions are dilute (low amino acid and dextrose concentration) precisely because concentrated, hypertonic solutions damage small peripheral veins. CPN solutions can be concentrated and hypertonic becausethey're infused into a large central vein with high blood flow that dilutes them immediately.
Adult PN is usually ordered on standardized paper or electronic forms, which cuts down on ordering, compounding, and administration errors. Pediatric PN is different: it's individualized and dosed per kilogram per day, and labeling should reflect that.
Macronutrients (water, protein, dextrose, lipid) supply energy (dextrose and lipid) and structural building blocks (protein and lipid).
| Component | Form | Calories | Key facts |
|---|---|---|---|
| Protein | Crystalline amino acids (CAAs) | 4 kcal/g | Whether protein calories count toward the total is debated; PN calories can be reported as total or nonprotein. Standard CAA products suit patients with normal organ function; specialty profiles exist for renal/hepatic disease. |
| Carbohydrate | Dextrose monohydrate, 5-70% concentrations | 3.4 kcal/g | The primary PN energy source |
| Lipid (ILE) | Lipid injectable emulsion | 9 kcal/g fat; 1.1 kcal/mL (10%), 2 kcal/mL (20%), 3 kcal/mL (30%) | Products differ in triglyceride source and essential fatty acid content; 30% ILE is TNA-only, not for direct infusion |
Give soybean oil ILE at 0.5-1 g/kg/dayin neonates/infants or 100 g/weekin adults, since linoleic and α-linolenic acid can't be made endogenously.
Mixing systems:10% and 20% ILE can run through a central or peripheral line, be compounded directly into the PN bag as a total nutrient admixture (TNA, the "three-in-one" of lipid/protein/dextrose plus additives), or co-infused separately alongside a CAA/dextrose solution (the "two-in-one"). 30% ILE is approved for TNA compounding only, never for direct infusion.
Micronutrients(vitamins, trace elements, electrolytes) support enzyme reactions, fluid balance, and electrophysiology. Standard multivitamin products are formulated separately for adults, children, and infants and include all 13 essential vitamins (including vitamin K). Copper, manganese, selenium, and zinc are the essential trace elements added as single- or multi-entity products. Sodium, potassium, calcium, magnesium, phosphorus, chloride, and acetate round out electrolyte needs, and how much of each depends on age, disease state, organ function, current medications, nutrition status, and ongoing losses outside the kidney.
| Parameter | During initiation | Once stable |
|---|---|---|
| Vital signs | Every 4-6 hours | As needed (e.g. new fever) |
| Weight | Daily | Weekly |
| Intake/output, tube-feeding intake, GI tolerance, tube/site checks | Daily | Daily |
| Electrolytes, BUN/SCr, glucose, Ca/Mg/Phos | Daily until stable | 2-3 times/week, then every 1-3 months |
| Liver function tests | Weekly | Every 1-3 months |
| Trace elements, vitamins | If deficiency or toxicity suspected | Same |
PN monitoring is more front-loaded than EN's. Baseline labs before starting, then daily checks for the first 3-4 days(electrolytes including sodium, potassium, chloride, bicarbonate, calcium, magnesium, phosphorus, plus serum glucose and kidney function), tapering to 2-3 times weekly once stable, with weekly liver function tests, nitrogen balance, and serum triglycerides. Critically ill patients may need more frequent checks than this baseline schedule; capillary glucose especially may need to be checked every 1-2 hours in unstable patients.
Add magnesium and phosphorusto the daily monitoring panel for anyone at risk for refeeding syndrome, or anyone whose baseline magnesium/phosphorus values were already abnormal. This is exactly why the first 3-4 days after starting PN get the tightest lab schedule of the whole course.
Also track:daily weight and vital signs, current nutritional intake, complete fluid balance (oral, nasointestinal, and IV in; urine, GI, and other losses out), CBC, serum albumin, and organ function markers (LFTs, BUN/SCr, PT/INR as needed). In pediatric patients, add total bilirubin daily in newborns until normal, serum triglycerides until stable on the maximum ILE dose, and height/length and head circumference tracking.